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Results for “TOXINS AND ANTITOXINS”

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At least 595 records · Page 33Linked to original sources
PubMed1984

The titration of tetanus antitoxin II. A comparative evaluation of the indirect haemagglutination and toxin neutralization tests.

Serum samples from 77 guinea pigs immunized against tetanus have been titrated for tetanus antitoxin by a standardized indirect haemagglutination (IHA) test and the conventional toxin neutralization (TN) test. These sera were titrated before and after treatment of the sera with 2-mercaptoethanol (2-ME) by the IHA test using unfixed sheep erythrocytes and erythrocytes fixed with glutaraldehyde, formaldehyde and pyruvic aldehyde. The titres of these sera obtained by IHA using unfixed and glutaraldehyde-fixed sheep erythrocytes before treatment of the sera with 2-ME were two to six times higher than the TN titres, whereas the IHA-titres using formaldehyde- and pyruvic aldehyde-fixed sheep erythrocytes were 10 times higher than the TN titres in some of the sera. There was no statistically significant difference between TN and IHA titres using unfixed and glutaraldehyde-fixed sheep erythrocytes after the treatment of the sera with 2-ME.

Animals↗
PubMed1963

Toxic effect of staphylococcal lysins for goldfish.

Goldfish died within 24 hr after intraperitoneal injections of 0.2 ml of Seitz filtrates of hemolytic Staphylococcus aureus cultures grown on Dolman and Wilson medium under increased CO(2) pressure for 72 to 96 hr. Two lethal toxins differing in heat sensitivity, antigenicity, and degree of toxicity were demonstrated. Studies of the relationship between the lethal factors and the hemolysins in the filtrates suggested that alpha- and beta-lysin were responsible for the lethal effects. Filtrates of nonhemolytic staphylococcal cultures were innocuous. Goldfish were suitable animals for detecting toxicity in staphylococcal culture filtrates and for quantitative studies of the toxins. The results were highly reproducible.

Animals↗
PubMed1961

The site of action of the Staphylococcus alpha toxin.

The present study concerns the site of action of the staphylococcus alpha toxin. This powerful necrotizing agent produced by pathogenic strains of staphylococcus is very probably important in the pathogenesis of localized staphylococcus disease and in the shock-like picture sometimes associated with staphylococcus septicemia. Our previous studies had suggested that the toxin has a selective effect on vascular smooth muscle. In investigating this problem further, the following observations were made. 1. The toxin produces an immediate hyperperistalsis and sustained increase in intraluminal tension progressing ultimately to atony and flaccid paralysis in the isolated smooth muscle preparation. 2. The addition of specific antitoxin prior to exposure to toxin prevents this reaction. However, when antitoxin is added after the toxin, no ameliorating effect is seen. 3. The toxin is rapidly and irreversibly bound to its substrate since washing the bowel segment 30 seconds after exposure to toxin fails to change the course of the reaction. 4. Vena caval segments exposed to toxin exhibit a similar initial rise in intraluminal tension followed by flaccid paralysis at which point they no longer respond to epinephrine stimulation. 5. When the toxin is infiltrated in the neighborhood of muscular blood vessels in the living rabbit selective necrosis of smooth muscle cells of the vessel walls is seen. 6. The selective effect on smooth muscle is emphasized by the failure of the toxin to affect the contractility of skeletal and cardiac muscle. 7. Perfusion of the isolated kidney and heart produces an increased resistance to flow after toxin is added to the perfusate. 8. Epithelial cells and fibroblasts in tissue culture exposed to high concentration of toxin for 2 hours are unaffected in their ability to recover and metabolise. This is in marked contrast to the effect on the smooth muscle preparation. The probability that the toxic effect on smooth muscle cells explains some of the local and systemic effects of staphylococcus infection is discussed.

Animals↗
PubMedDate not supplied

Pertussis toxin: the cause of the harmful effects and prolonged immunity of whooping cough. A hypothesis.

The nature of the pathogenesis and of the prolonged immunity of whooping cough has not been clearly defined. The literature of Bordetella pertussis indicated that only the antigen that induces histamine sensitization, lymphocytosis, and other biological reactions in mice is the cause of the harmful effects and prolonged immunity of whooping cough. This antigen has the general characteristics of bacterial protein exotoxins that cause the harmful effects of infectious diseases such as diphtheria and tetanus. It is proposed that this antigen, which is histamine-sensitizing, lymphocyte-leukocyte-promoting, and islets-activating (HSF-LPF-IAP), be designated pertussis toxin. Agglutinogen, hemagglutinin, and heat-labile (at 56 C) and heat-stable (at 100 C) toxins are no doubt interrelated with the immunologic and/or toxic reactions of whooping cough. It appears that the first defense against the disease is the antibody that prevents adhesion of the bacteria to the cilia of the respiratory epithelium and that the second defense is the antitoxin against pertussis toxin (HSF-LPF-IAP).

Agglutinins↗
PubMed1985

Protection of the nursing pig against experimentally induced enteric colibacillosis by vaccination of dam with fimbrial antigens of E coli (K88, K99 and 987P).

Pregnant gilts were vaccinated with two doses of alhydrogel adsorbed fimbrial antigens of Escherichia coli (K88ab, K88ac, K99 and 987P) supplemented with beta toxoid of Clostridium perfringens type C. Their piglets, and piglets of nonvaccinated gilts, were subsequently orogastrically challenged with one or other of the four fimbrial types of enteropathogenic E coli. Some of the vaccinated animals were reinjected with a single dose of the vaccine during second gestation and their piglets, and piglets of non-vaccinated sows, were challenged the same way as were litters of gilts. Blood serum and colostra were examined for antibodies to the four fimbrial antigens of E coli and for antitoxin to beta toxin of C perfringens type C. It was found that: (1) a highly significant reduction in mortality and morbidity was achieved in vaccinated litters against all four challenge strains of E coli; (2) excretion of K88ab and K88ac but not of K99 and 987P challenge strains was significantly reduced; (3) revaccination of sows by a single dose of the vaccine during second gestation conferred complete protection against mortality and highly significant protection against morbidity; (4) no correlation was noted between colostral or seroagglutinins to fimbrial antigens of E coli and mortality rates in litters challenged with homologous fimbrial types of E coli, but good correlation was found between colostral precipitins to K88 antigens and mortality rates in litters; (5) antitoxin value in 97 per cent of colostrum of vaccinated sows was 10 iu equivalent of C perfringens type C toxin or more per ml of colostrum.

Adhesins, Escherichia coli↗